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Anatomy and Physiology: Muscles

by: Jeni Erickson

Anatomy and Physiology: Muscles 80197 - BIOL 2220 - 001

Marketplace > Clemson University > 80197 - BIOL 2220 - 001 > Anatomy and Physiology Muscles
Jeni Erickson
GPA 3.7

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Muscle Contractions
Human Anatomy and Physiology I
John R Cummings
Class Notes
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This 5 page Class Notes was uploaded by Jeni Erickson on Monday October 17, 2016. The Class Notes belongs to 80197 - BIOL 2220 - 001 at Clemson University taught by John R Cummings in Fall 2016. Since its upload, it has received 3 views.

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Date Created: 10/17/16
 Requirements fro Resting State o Oxygen is stored in myoglobin. Oxygen binds to hemoglobin, travels to the muscle, and binds to the myoglobin. o Oxygen reserves must be replenished o Lactic acid must be converted to pyruvic acid, glucose or glycogen  Glucose is converted to glycogen and then stored. o Glycogen stores must be replaced o ATP reserve must be resynthesized  If muscle becomes fatigue, it stays in a contracted state and causes cramping. o Creatine phosphate reserve must be resynthesized  We don’t replenish these directly as a creatine phosphate.  Creatine is delivered to the muscle cell from things we eat.  Then phosphate is delivered to the muscle cell and binds to creatine.  Force of Contraction/Tension on a muscle o Number of fibers stimulated/number of motor units activated: the more fibers stimulated, the stronger the contraction. o Relative size of fibers: we are basically born with all the muscle cells that we are going to have. The size of the muscle is what makes us stronger or weaker. The bigger the size, the stronger the contraction is. o Frequency of stimulation: if we don’t allow the muscle to contract, then the contraction is stronger. o Degree of stretch: the amount of overlap between thick and thin myofilaments.  Minimal overlap has the strongest contraction.  Too much of strength does not allow for a strong muscle contraction.  If they are too overlapped, the muscle can’t contract anymore. Speed of the contraction of the fiber and how ATP is produced  Types of Muscle Fibers: Genetics determine to proportion of these that we have in our body. If we have more myoglobin, more oxygen is stored and we can use slow oxidative fibers. o Slow oxidative fibers  Splits ATP slowly and contracts slowly. Uses an aerobic pathway. Resistant to fatigue. Produces a lot of ATP. Doesn’t contract rapidly, but can contract continually.  Long distance runner. o Fast oxidative fibers:  Splits ATP rapidly. Relatively resistant to fatigue. Muscle contraction is rapid.  Sprinter (400 meter person) o Fast glycolytic fibers: Will just use glycolysis. Anaerobic and fatigues easily. Rapid contraction for a short duration.  Effects of Exercise: o Aerobic exercise: primarily uses slow oxidative fibers because you do this for a longer duration. It brings on endurance. Angiogenesis occurs, which is when the body builds/develops new capillaries so that oxygen can move around more and quicker. Mitochondria per muscle cell increases so that we can produce more energy. Increase of myoglobin stored inside the cell. o Resistance exercise: increase in power. Rely primarily of fast glycolytic fibers. Anaerobic pathway. Hypertrophy- increases the size of the muscle cells. Doesn’t have a lot of myoglobin. We increase the proteins composition of a muscle in order to make the cells bigger. o Disuse atrophy: we can’t use our muscles for a while. As soon as we stop using a muscle (the very second), the muscle fibers diminish in size. IF there is a long-term disuse of muscle, the muscle tissue will convert to fibrous connective tissue. Skeletal muscle will change into dense irregular connective tissue. You will lose muscle ability permanently. Cardiac muscle behaves very similarly to skeletal muscle.  Smooth Muscle o Completely involuntary o Fibers smaller than skeletal  They are much smaller and shorter. Does not go the full length of the muscle. o Lack connective tissue sheaths  They do have endomysium but no epimysium o Organized into sheets  Longitudinal layer   Circular layer o Unstructured neuromuscular junction  Instead of it being a somatic neuron, it is an autonomic nerve fiber. There is no modification on the surface of the muscle. The nerve fiber contains vesicles and neurotransmitters that diffuse across the synaptic cleft. Receptors are found in different places compared to skeletal muscle.  Autonomic have bulbus varicosities.  Release neurotransmitters into diffuse junctions. o There is no end plate and no modifications on the sarcolemma.  They web around the muscle.  There can be receptors at any point around the muscle cells because of the web around the muscle of varicosities.  Less developed sarcoplasmic reticulum. It touches the sarcolemma at multiple sites.  In skeletal muscle the sarcoplasmic reticulum stored calcium, but not really in smooth muscle. It is mostly stored on the outside of the cell. o Smooth Muscle SR  No sarcomeres  No pattern to myofilaments  No T tubules  Instead it has caveoli: these pouches concentrate calcium outside of the cell and holds it close to the cell. o Myofilament Arrangement  Contains both think and thin myofilaments  10-15 thin myofilaments for each long thick myofilament  Myosin heads found along entire length of thick myofilament, not just at the ends.  Tropomyosin associated with thin myofilament, but no troponin. There is nothing to cover up the actin- binding site.  Myofilaments generally run diagonally across the cell (within fibers).  Contain intermediate filaments: These attach in various locations across the cell.  They attach from one dense body to another dense body. It gives the contractile elements something to pull against.  Types of Smooth muscle o Visceral smooth muscle:  Contracts as a unit and does so rhythmically.  Has gap junctions  Lines the hollow organs in the body. o Multiunit  Found in a lot of different places  Arrector Pilli muscle, large arteries, eye muscles.  Smooth Muscle Contraction o Neurotransmitter (not always acetyl choline) stimulates production of action potential  Defuses across cleft and binds to sarcolemma.  Sodium channels open  Membrane of sarcolemma changes permeability  Sodium depolarizes the resting neuron o Calcium is released by caveoli  More importantly is taken in from extracellular space  Calcium can now move in to cell because of the change in sarcolemma permeability. o Calcium binds to calmodulin. This is a calcium binding protein found inside the cell.  Calmodulin is activated o Activated calmodulin activates myosin light chain kinase (ATPase- splits ATP) o Activated kinase changes the myosin cross bridges and puts it in high-energy configuration. o Actin and myosin interact to shorten fibers o When calcium is pumped out of cell, the ATP binds with myosin so it cant interact with actin and we enter relaxation.  Regulation of Contraction o Autonomic nerves release different neurotransmitters.  We have an “on” neurotransmitter and an “off” neurotransmitter. o Chemical factors  Will affect the movement of calcium into the cell (excites or inhibits)  Hormones  pH changes stuff for muscle contractions  Development of Muscle o Mesodermal origin o Skeletal myoblasts fuse o Cardiac and smooth do not o Cardiac and smooth both form gap junctions. o Agrin clusters and maintains ACh receptors  Growth factor released by spinal nerves.  It creates motor end plates on skeletal muscle.  Ach receptors get lost entirely in smooth muscle.


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